Shannon et al. (42) demonstrated that a specific TRPV4 antagonist, GSK2193874, was able to attenuate aortic growth and decrease pro-inflammatory cytokines in both angiotensin II (AngII)-induced AAA in ApoE–/– mice and in ECs in culture, thereby reducing the activation of SMCs and trans-endothelial migration during AAA formation (Table 1 and Figure 2). The gene discussed is TRPV4; the disease is triple-A syndrome.